Immunoregulatory cytokine changes result from HIV infection, with decreased type 1 cytokines that enhance cellular immunity (CI) and increased type 2 cytokines that augment humoral immunity (HI). IL-12 and IL-10 increase and decrease CI, respectively, and are produced by APC that are monocytes (MC) and dendritic cells (DC), important targets of HIV infection. MC from HIV+ patients produced reduced levels of IL- 12 and increased levels of IL-10, as did MC infected in vitro with HIV. In contrast, DC appeared to be resistant to HIV-induced cytokine changes. Therapeutic trials of pediatric AIDS patients with highly active anti-retroviral therapy (HAART) indicated that patients who presented with reduced viral loads and increased CD4 counts did not exhibit normalized IL-12 and IL-10 production. This finding suggests that multi-drug therapy-induced changes in CD4 count and viral load is not reflected in improved immune function. In vitro production of IL-12 by MC of HIV+ patients was restored by the synergistic effects of IFN- gamma and CD40 ligand, suggesting that this combination might be used in therapeutic trials. MC from uninfected newborns of HIV-infected mothers did not produce IL-12, in contrast to the MC of newborns of HIV uninfected mothers that did produce IL-12. Stimulation of PBMC with allogeneic leukocytes resulted in the production of IL-2, which was responsible for by-passing an induced defect in the CD80/86~CD28 costimulatory pathway. This defect is characteristic of immune dysregulation in HIV/AIDS. Stimulation of PBMC from HIV- control donors and some HIV+ patients with influenza A virus (Flu) results in the production of multiple anti-HIV factors that inhibit both CCR5- and CXCR4-using viral isolates at different points in the HIV replication cycle. These factors are produced by either CD4- or CD8-depleted PBMC cultures. Stimulation of PBMC with allogeneic leukocytes also results in the production of multiple anti-HIV factors. Efficient allo- stimulated anti-HIV factor production appears to be HLA associated, with the HLA-A2 allele conferring potent factor production. AZT was incorporated into the fetal cord blood leukocytes from a majority of women who received AZT during pregnancy. Based on experience from a murine model, this finding raises the possibility of long-term AZT- induced carcinogenesis in the offspring. Immunization of SIV-infected macaques with a poxvirus vector expressing SIV gag, pol and env genes protected against viral rebound when anti-retroviral therapy was withdrawn, and raised the possibility of this strategy for immune-based therapy. Mice transfected with the entire HIV-1 genome expressed virus in their monocytes but not in their T cells when infected with murine pathogens.AIDS Title: Immune Dysregulation In HIV/AIDS - AIDS, Cytokines, genes, HIV, T cells, HLA, antigen-presenting cells, - Human Tissues, Fluids, Cells, etc.